摘要：SummaryIgE and IgG1 production in the type 2 immune response is the characteristic feature of an allergic reaction. However, whether bacterial molecules modulate IgE and IgG1 production remains obscure. Here, we demonstrate that the bacterial quorum sensing molecules acyl homoserine lactones (AHLs) induce IgE and IgG1 production by activating the RARE (retinoic acid response element) response in dendritic cells (DCs)in vivo. DC-specific knockout of the retinoic acid transcriptional factor Rara diminished the AHL-stimulated type 2 immune responsein vitro. AHLs altered DC phenotype, upregulated OX40L and IFN-I signature, and promoted T helper 2 cell differentiationin vitro. Finally, AHLs activated the RARE response by inhibiting AKT phosphorylationin vitro, as the AKT agonists IGF-1 and PDGF abolished the effect of AHLs on the RARE response. This study demonstrates a mechanism by which AHLs drive allergic airway inflammation through activating retinoic acid signaling in DCs.Graphical AbstractDisplay OmittedHighlights•Acyl homoserine lactones (AHLs) exacerbate allergic airway inflammation•AHLs induce IgE and IgG1 production•AHLs activate the RARE response in dendritic cells•AHLs inhibit AKT phosphorylationBiological Sciences; Immunology; Immune Response
